Pediatric respiratory syncytial viral infection (RS) usually shows </span><span style="font-family:Verdana;">relatively</span><span style="font-family:Verdana;"> good </s...Pediatric respiratory syncytial viral infection (RS) usually shows </span><span style="font-family:Verdana;">relatively</span><span style="font-family:Verdana;"> good </span><span style="font-family:Verdana;">outcome</span><span style="font-family:Verdana;">;however, when it accompanies acute respiratory distress syndrome (ARDS), this becomes fatal. We experienced three pediatric patients with RS + ARDS, with all showing good </span><span style="font-family:Verdana;">outcome</span><span style="font-family:Verdana;"> with steroid pulse therapy. We wish to emphasize;1) steroid pulse therapy may become an option for this condition, and 2) plasma KL-6 and surfactant protein D levels may become a biomarker reflecting the disease progression/condition. Patients were, aged 1 month, 1 year 5 months, and 1 year 11 months. In all three, the respiratory condition deteriorated rapidly, requiring invasive ventilator management. Although the effectiveness of steroid treatment for ARDS is controversial, </span><span style="font-family:Verdana;">very</span><span style="font-family:Verdana;"> severe condition prompted us to employ steroid pulse therapy, after which, oxygenation rapidly improved without adverse events. Plasma KL-6 and surfactant protein D levels were measured during exacerbations of ARDS, steroid pulse therapy, and recovery. Surfactant protein D levels were closely associated with oxygenation, suggesting this substance level might be a biomarker of ARDS caused by the disruption of the alveolar epithelial lining and to understand oxygenation without time lag.展开更多
Increased levels of surfactant protein D (SP-D) and lipid-laden foamy macrophages (FMs) are frequently found under oxidative stress conditions and/or in patients with chronic obstructive pulmonary disease (COPD) who a...Increased levels of surfactant protein D (SP-D) and lipid-laden foamy macrophages (FMs) are frequently found under oxidative stress conditions and/or in patients with chronic obstructive pulmonary disease (COPD) who are also chronically exposed to cigarette smoke (CS). However, the roles and molecular mechanisms of SP-D and FMs in COPD have not yet been determined. In this study, increased levels of SP-D were found in the bronchoalveolar lavage fluid (BALF) and sera of ozone- and CS-exposed mice. Furthermore, SP-D-knockout mice showed increased lipid-laden FMs and airway inflammation caused by ozone and CS exposure, similar to that exhibited by our study cohort of chronic smokers and COPD patients. We also showed that an exogenous recombinant fragment of human SP-D (rfhSP-D) prevented the formation of oxidized low-density lipoprotein (oxLDL)-induced FMs in vitro and reversed the airway inflammation and emphysematous changes caused by oxidative stress and CS exposure in vivo. SP-D upregulated bone marrow-derived macrophage (BMDM) expression of genes involved in countering the oxidative stress and lipid metabolism perturbations induced by CS and oxLDL. Our study demonstrates the crucial roles of SP-D in the lipid homeostasis of dysfunctional alveolar macrophages caused by ozone and CS exposure in experimental mouse emphysema, which may provide a novel opportunity for the clinical application of SP-D in patients with COPD.展开更多
文摘Pediatric respiratory syncytial viral infection (RS) usually shows </span><span style="font-family:Verdana;">relatively</span><span style="font-family:Verdana;"> good </span><span style="font-family:Verdana;">outcome</span><span style="font-family:Verdana;">;however, when it accompanies acute respiratory distress syndrome (ARDS), this becomes fatal. We experienced three pediatric patients with RS + ARDS, with all showing good </span><span style="font-family:Verdana;">outcome</span><span style="font-family:Verdana;"> with steroid pulse therapy. We wish to emphasize;1) steroid pulse therapy may become an option for this condition, and 2) plasma KL-6 and surfactant protein D levels may become a biomarker reflecting the disease progression/condition. Patients were, aged 1 month, 1 year 5 months, and 1 year 11 months. In all three, the respiratory condition deteriorated rapidly, requiring invasive ventilator management. Although the effectiveness of steroid treatment for ARDS is controversial, </span><span style="font-family:Verdana;">very</span><span style="font-family:Verdana;"> severe condition prompted us to employ steroid pulse therapy, after which, oxygenation rapidly improved without adverse events. Plasma KL-6 and surfactant protein D levels were measured during exacerbations of ARDS, steroid pulse therapy, and recovery. Surfactant protein D levels were closely associated with oxygenation, suggesting this substance level might be a biomarker of ARDS caused by the disruption of the alveolar epithelial lining and to understand oxygenation without time lag.
基金supported by the Ministry of Science and Technology(MOST)of Taiwan(grant numbers 103-2321-B-006-030 and 104-2321-B-006-008),funding received in part from the Headquarters of University Advancement at the National Cheng Kung University,which is sponsored by the Ministry of Education in Taiwan,and a research grant(1JA8)from the Center for Allergy,Immunology,and Microbiome(A.I.M.),China Medical University Hospital,Taichung,Taiwan.
文摘Increased levels of surfactant protein D (SP-D) and lipid-laden foamy macrophages (FMs) are frequently found under oxidative stress conditions and/or in patients with chronic obstructive pulmonary disease (COPD) who are also chronically exposed to cigarette smoke (CS). However, the roles and molecular mechanisms of SP-D and FMs in COPD have not yet been determined. In this study, increased levels of SP-D were found in the bronchoalveolar lavage fluid (BALF) and sera of ozone- and CS-exposed mice. Furthermore, SP-D-knockout mice showed increased lipid-laden FMs and airway inflammation caused by ozone and CS exposure, similar to that exhibited by our study cohort of chronic smokers and COPD patients. We also showed that an exogenous recombinant fragment of human SP-D (rfhSP-D) prevented the formation of oxidized low-density lipoprotein (oxLDL)-induced FMs in vitro and reversed the airway inflammation and emphysematous changes caused by oxidative stress and CS exposure in vivo. SP-D upregulated bone marrow-derived macrophage (BMDM) expression of genes involved in countering the oxidative stress and lipid metabolism perturbations induced by CS and oxLDL. Our study demonstrates the crucial roles of SP-D in the lipid homeostasis of dysfunctional alveolar macrophages caused by ozone and CS exposure in experimental mouse emphysema, which may provide a novel opportunity for the clinical application of SP-D in patients with COPD.